Nordmark J, Rydqvist B
Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
Neuroreport. 1997 Jan 20;8(2):465-8. doi: 10.1097/00001756-199701200-00018.
A two-electrode voltage clamp was used to examine the effects of the local anaesthetics (LAs) lidocaine, tetracaine and bupivacaine, and the meta-isomer of lidocaine (LL33), on the gamma-aminobutyric acid (GABA)-gated Cl- channel in the crayfish stretch receptor neurone. The voltage-induced current changes were recorded while exposing the neurone to GABA in saline containing different LAs. All LAs enhanced the voltage-induced Cl- current equivalent to a shift of the conductance vs GABA curve towards lower concentrations. The mechanism of the facilitation of GABA-induced conductance was found to be mainly a block of the GABA uptake in the stretch receptor neurone. Tetracaine, and to a lesser extent LL33, also seem to affect directly the GABA/receptor Cl-/channel complex resulting in an increased conductance of the channel.
采用双电极电压钳技术，研究了局部麻醉药（LAs）利多卡因、丁卡因和布比卡因以及利多卡因的间位异构体（LL33）对小龙虾牵张感受器神经元中γ-氨基丁酸（GABA）门控氯离子通道的影响。在含有不同局部麻醉药的盐溶液中，将神经元暴露于GABA时，记录电压诱导的电流变化。所有局部麻醉药均增强了电压诱导的氯离子电流，相当于电导与GABA曲线向更低浓度偏移。发现GABA诱导电导增强的机制主要是牵张感受器神经元中GABA摄取的阻断。丁卡因以及程度较轻的LL33似乎也直接影响GABA/受体-Cl-/通道复合物，导致通道电导增加。
